Interaction of lincRNA ROR and p53/miR-145 correlates with lung cancer stem cell signatures.

ROR is one of large intergenic non-coding RNAs (lincRNAs) and acts as a strong negative regulator of p53 and a sponge for miR-145 to regulate diverse cancer progression. However, the interaction of ROR, p53 and miR-145 in lung cancer and its correlation with lung cancer stem cell (LCSC) signatures were not fully understood. Here, qRT-PCR analysis revealed that p53 and ROR were upregulated while miR-145 was downregulated in non-small cell lung cancer (NSCLC) tissues and LCSCs compared to their paired adjacent normal tissues and lung cancer cells (LCCs). Besides, high p53 level, low miR-145 level, and high ROR level were associated with poor prognosis in NSCLC. Then, we found that silencing ROR failed to change p53 mRNA level but promoted p53 protein level, suggesting a posttranscriptional regulation mechanism involved in si-ROR-mediated promotion of p53. While silencing p53 moderately downregulated ROR. Additionally, silencing ROR or p53 upregulated miR-145. However, silencing both ROR and p53 failed to make obvious change to miR-145 mRNA level and p53 protein level. And interestingly, miR-145 negatively regulated Oct4 and Sox2. We also found that silencing ROR and (or) p53 suppressed in vitro cell proliferation, migration and invasion in LCSCs and LCCs. And suppression of endogenous ROR reduced the in vivo tumor growth and metastasis of LCSCs. Our study demonstrated that ROR and p53/miR-145 correlated with prognosis in NSCLC as well as cell proliferation, migration, invasion, and tumorigenicity of LCSCs, shedding new light on novel therapeutic options in lung cancer. This article is protected by copyright. All rights reserved.